Oral candidiasis is a common opportunistic fungal infection of the oral mucosa, primarily caused by Candida species, particularly Candida albicans, which normally resides as a commensal organism in the oral cavity, gastrointestinal tract, and genitourinary mucosa.^1,2 Candida exhibits dimorphism and exists in both yeast (blastospore) and hyphal (mycelial) forms. Although the yeast form is typically non-pathogenic, the hyphal form is associated with tissue invasion, making this morphological transition an important factor in the diagnosis and management of candidal infections.³

Under normal physiological conditions, Candida growth is regulated by host immune defenses, salivary antimicrobial factors, and the oral microbiota balance. Disruption of these protective mechanisms may facilitate Candida to shift from a commensal organism to an opportunistic pathogen capable of causing mucosal infection.⁴

Predisposing factors such as immunosuppression, diabetes mellitus, prolonged antibiotic or corticosteroid therapy, xerostomia, denture use, poor oral hygiene, and systemic conditions, including human immunodeficiency virus (HIV) infection or malignancy, can markedly increase the risk of oral candidiasis.⁵ These factors highlight the need to evaluate both local determinants, such as the surface characteristics of dental prostheses that promote microbial adhesion, as well as systemic host susceptibility.^6,7

The pathogenic potential of Candida species is multifactorial and driven by a range of virulence factors that enable colonization, tissue invasion, and persistence within host tissues.^8,9

Candida albicans displays pathogenic potential through morphological switching from yeast to hyphal forms, a transition that facilitates epithelial invasion and deeper tissue penetration.¹⁰ Moreover, processes such as molecular mimicry and phenotypic switching allow the organism to evade host immune responses and persist within host tissues despite a functional innate immune system.¹¹

Candida produces surface adhesins that promote adherence to epithelial cells, dental surfaces, and prosthetic materials, such as dentures, thereby facilitating colonization and biofilm development. These biofilms shield the organism from the host immune defenses and antifungal therapies, contributing to microbial persistence and treatment resistance.¹²

Candida secretes hydrolytic enzymes, such as secreted aspartyl proteases, lipases, and phospholipases, which degrade host tissues and extracellular matrix components, thereby facilitating mucosal invasion and inflammation.¹³ Host immune responses play a crucial role in controlling infection, with both innate and adaptive immune mechanisms, particularly those mediated by neutrophils, macrophages, and T lymphocytes, contributing to antifungal defense.¹⁴ The cytolytic peptide toxin candidalysin further intensifies this process by causing epithelial cell damage and activating pro-inflammatory signaling pathways.¹⁵

Oral candidiasis may manifest in several clinical forms, including acute pseudomembranous candidiasis (oral thrush), acute erythematous candidiasis, chronic erythematous candidiasis, median rhomboid glossitis, angular cheilitis, and chronic hyperplastic candidiasis, reflecting variations in the host immune status and pathogen-host interactions.^3,12

Oral thrush, also known as acute pseudomembranous candidiasis, is the most common clinical presentation of oral candidiasis. It typically manifests as soft, curdy-white plaque-like lesions on the oral mucosa, frequently involving the dorsum of the tongue, buccal mucosa, palate, and oropharynx.¹⁶ These plaques comprise fungal hyphae, epithelial debris, inflammatory cells, and fibrin, and can be easily removed to demonstrate an underlying erythematous mucosal surface. Patients may present with burning sensation, dysgeusia, or oral discomfort, although some may remain asymptomatic.¹⁷

Acute pseudomembranous candidiasis frequently occurs in infants, older adults, and immunocompromised individuals, and is associated with the use of antibiotics, corticosteroids, chemotherapy, or other immunosuppressive therapies.²

Early diagnosis and timely management are important to prevent disease progression and potential systemic complications. Management typically involves topical or systemic antifungal therapy, along with addressing underlying predisposing factors. Therefore, the effective diagnosis and management of oral candidiasis in dental and medical practice rely on a clear understanding of its pathogenic mechanisms and clinical manifestations.^17,18

Recent research has highlighted the potential of medicinal plants and nutraceuticals as cost-effective therapeutic regimens.¹⁹ Concurrently, the alarming rise in antifungal resistance necessitates the exploration of novel treatment strategies and probiotic adjuncts, along with a deeper understanding of the interactions between non-albicans Candida species and patient-specific risk factors to optimize clinical outcomes.^20,21

Case scenario

A 37 year-old female patient was referred to our outpatient department with the chief complaint of a burning sensation in the oral cavity for the past two months. The patient described the burning sensation as continuous in nature and was aggravated during food intake, particularly with spicy or acidic foods.

The patient’s medical history was significant for bronchial asthma, for which she had been prescribed an inhaled bronchodilator containing low-dose budesonide (corticosteroid) and formoterol (long-acting β-agonist) for the past six months. The medication was administered using a metered-dose inhaler (MDI); however, the patient reported that she had not received proper instructions regarding the inhalation technique and she admitted to frequent inhaler use without routinely rinsing her mouth after inhalation.

The patient denied a history of diabetes mellitus, immunosuppressive therapy, recent systemic illness, prolonged antibiotic use, tobacco use, or alcohol consumption. Her dietary habits were normal and no significant weight loss or systemic symptoms were reported.

The results of the general physical and extraoral examinations were unremarkable. Intraoral examination revealed curdy white plaque-like lesions involving the anterior and middle thirds of the tongue dorsum. The lesions exhibited an irregular distribution pattern, mimicking a coated tongue (Figure 1a). Whitish pseudomembranous patchy plaques interspersed with areas of mild erythema were observed on the hard palate and adjoining palatal mucosa (Figure 1b). The right buccal mucosa exhibited thin irregular white patches over an erythematous mucosal background extending from the commissural region to the posterior buccal mucosa (Figure 1c). Similar white pseudomembranous plaque lesions were observed in the left buccal mucosa and retromolar region (Figure 1d). The lesions were soft, superficial, homogeneous, and loosely adherent. Gentle scraping resulted in partial plaque removal, leaving an erythematous and mildly inflamed mucosal surface.

The mouth mirror test revealed xerostomia. The patient reported a marked oral burning sensation with a visual analog scale (VAS) score of 7.

In addition, multiple root stumps, grossly decayed teeth, and poor oral hygiene were observed, which could potentially contribute to microbial colonization and opportunistic infections.

The patient’s clinical presentation of multifocal scrapable white plaque lesions, together with a history of corticosteroid inhaler use without proper oral hygiene, strongly suggested acute pseudomembranous candidiasis.

Differential diagnoses included oral lichen planus, oral leukoplakia, coated tongue, oral hairy leukoplakia, and chemical burns. However, unlike these conditions, pseudomembranous candidiasis typically presents as soft, creamy white plaques that can be easily scraped off, leaving beneath an erythematous or occasionally bleeding mucosal surface.

A complete hemogram and rapid human immunodeficiency virus (HIV) test were performed to exclude systemic involvement. These investigations revealed values within normal limits and a non-reactive HIV status.

A smear of the lesion was collected for microscopic evaluation. Hematoxylin and eosin (H&E; 10×) stained sections showed numerous thin-walled filamentous structures suggestive of fungal hyphae (Figure 2a).

At a higher magnification (H&E; 40×), the sections demonstrated multiple neutrophilic microabscesses within the superficial epithelial layers, indicating an acute inflammatory response associated with fungal infection (Figure 2b).

Further confirmation was obtained using periodic acid-Schiff (PAS) staining, which demonstrated magenta-colored tubular hyphal structures consistent with Candida species invading the superficial epithelial layers (Figure 2c). The presence of PAS-positive fungal elements within the epithelium confirmed oral candidiasis.

The patient was prescribed systemic antifungal therapy with oral fluconazole, administered at 200 mg on the first day, followed by 100 mg once daily for the next 10 days, along with topical Clotrimazole therapy (Candid mouth paint 1%) for local application three times daily for 10 days. The patient was also advised to use Coolora mouthwash (Benzydamine Hydrochloride 0.15% w/v) as an adjunct to maintain oral hygiene and reduce the microbial load.

The patient received instructions on the maintenance of oral hygiene, including regular tooth brushing and plaque control. She was advised to rinse her mouth thoroughly after the use of inhaled bronchodilators and to use a spacer with her corticosteroid inhaler to reduce medication deposition in the oropharyngeal region. Dental treatment for multiple carious teeth and root stumps was recommended.

At the 10 day follow-up visit, the patient reported a huge relief from the burning sensation, and clinical examination revealed complete resolution of the lesions (Figures 3a-d).

At the 2 month follow-up, the patient remained asymptomatic and clinical examination revealed no recurrence of candidiasis.